BY: DR.

AMMARAH YASMEEN HOUSE OFFICER MEDICAL UNIT IV CHK

Define basic terms. Explain neuroanatomy precisely. Review causes of unconsciousness. Clinical approach to follow in E.R. Review key aspects of history, physical examination and lab evaluation. Definitive management.

It has been defined, at one time or another, as: subjective experience; awareness; the ability to experience feelings; wakefulness; having a sense of selfhood; or as the executive control system of the mind. Two components of conscious behavior The three most widely accepted states of consciousness are sleeping, dreaming and waking.

content- the sum of cognitive and affective function arousal- appearance of wakefulness

DROWSINESS:

A decreased level of consciousness characterized by sleepiness and difficulty in remaining alert but easy arousal by stimuli. It may be caused by a lack of sleep, medications, substance abuse, or a cerebral disorder.

OBTUNDATION:

A greatly reduced level of consciousness. The patient is not yet comatose but is close, arousing only with very strong stimulus.

STUPOR: COMA:

A state of impaired consciousness characterized by a marked diminution in the capacity to react to environmental stimuli. Is a state of extreme unresponsiveness, in which an individual exhibits no voluntary movement or behavior.

Unconsciousness implies a mental state that involves complete or near-complete lack of responsiveness to people and other environmental stimuli. Being in a comatose state or coma is a type of unconsciousness.

Wakefulness depends on the integrity of both cerebral hemispheres and the ascending reticular activating formation of the brain stem. It receives input from numerous somatic afferents. It projects to midline thalamic nuclei (which are in a circuit with cortical structures) and the limbic system.

ARAS acts as a gating system, increasing or decreasing thalamic inhibitory influence on the cortex
alters effect of sensory stimuli ascending alters descending cortical stimulation

Function of ARAS-Thalamic-Cortical system depends on:

anatomic integrity of structures metabolic integrity (circulatory integrity) communicative integrity (neurotransmitter function)

Coma (unconsciousness) implies dysfunction of:

ARAS or Both hemi-cortices

Anatomically, this means

Central brainstem structures (bilaterally) from caudal medulla to rostral midbrain Both hemispheres

Thiamine deficiency Brain tumor metabolic disturbances

Causes of unconciousness

epilepsy

trauma

infections

Cardiovascular disease

NEUROLOGICAL

Trauma Infections meningitis, encephalitis, malaria, typhoid, rabies, trypanosomiasis. Tumours cerebral / meningeal tumors Vascular subdural / subarachnoid hgr, stroke, hypertensive encephalopathy Epilepsy nonconvulsive status / postictal state

METABOLIC

Drugs, poisoning e.g CO ,alcohol etc. Hypoglcemia, hyperglycemia (keto acidoti or HONK) Hypoxia, carbondiaoxide narcosis (COPD) Septicemia Hypothermia Myxedema ,addisonian crisis Hepatic / uremic encephalopathy Thiamine deficinecy

CARDIOVASCULAR

Cardiac arrest

OTHERS

Stroke(hypovolemic), syncope, Psychogenic (hysteric)

ABC Immediate management

History
Examination Investigations

ABC

A Open the airway

Examining the Airway for obstruction and Cervical Spine Control in the event of any possible trauma for e.g fracture. Maintain airway.oropharyngeal endotracheal.

B breathing
Breathing shallow.?........ Aspiration? Look, Listen and Feel for adequate respiratory effort. Supplement with O2 to correct hypoxia if saturations are below 95%.

C circulation
If trauma check for bleeding then checking the circulation. If a carotid pulse is not palpable then resuscitation should be commenced.

Maintain i.v line and support the ciculation if required with I.V fluids. oxygen inhalation Protect the cervical spine unless trauma is known not to be the cause.

Check blood glucose; give 50mL 50% dextrose IV stat if hypoglycemia is possible.

I.V thiamine if history of alcohlism. Control and treat seizures if present.

I.V naloxone (0.4mg-2mg IV) for opiate intoxication; I.V flumazenil for benzodiazepine intoxication.

HISTORY

Onset of symptoms (abrupt or gradual) How found suicide note, seizures. Fever Headache Vomiting.types.. Trauma Recent altered behaviour..? H/o diabetes? Hypertension? controlled? Poison..? Prior suicidal attempts?


o o o

Drugs?

o
o o

Insulin, OHA Antipsychotics Sedatives Steroids Anti coagulants Diuretics

Acute or Chronic alcohol intake Seizure disorder Prior episode of coma Elderly nothing predictable Past medical history- chronic liver ,kidney ,lung, heart disease, diabetes or psychiatric illness.

EXAMINATION

APPEARANCE

o o o o

ODOR
Alcohol Fruity .DKA Uriniferous .Uremia Musty fetor of Hepatic coma Burnt almond odor of Cyanide Organophosphate

o
o

COLOUR

Pallor Severe internal hemorrhage, Hypothyroidism , Hypopituitarism , CKD o Cyanosis of lips and nails o Cherry red.CO o Facial plethora . alcoholism o Maculo hemorrhagic rash Meningococcemia , Typhus, RMSF, Staph endocarditis

DIFFUSE PETECHIAE

-TTP, DIC, Fat embolism

ECHYMOTIC PATCHES

-Drug induced -CLD -DIC -Trauma

LARGE BLISTERS

-If the patient has been motionless for a time -Acute barbiturate, alcohol, or opiate intoxication

FACIAL PUFFINESS

-CKD -Myxedema, Hypopituitarism

NAIL

-Splinter hemorrhage -White nail -Half and half nail -Clubbing

FEVER
Jaundice Features of chronic liver disease

-Pneumonia, sepsis, meningitis

Central obesity, striae

Nasal bleed, CSF leak Aural bleed

1.PULSE

VITALS
Tachycardia

Hypovolemia/haemorrhage Hyperthermia Intoxication Bradycardia Raised intracranial pressure Heart blocks

2. TEMPERATURE
Increased

Sepsis Meningitis ,encephalitis Malaria ,Pontine haemorrhage Drugs with anticholinergic activity Heat stroke Decreased

Hypoglycemia Hypothermia (less than 31 C) Myxedema Alcohol, barbiturate ,sedative or phenothiazine intoxication.

3.BLOOD PRESSURE
Increased

Hypertensive encephalopathy Cerebral haemorrhage Raised intracranial pressure Decreased

Hypovolemia Myocardial infarction Intoxication/poisoning Profound hypothyroidism, Addisonian crisis

4. RESPIRATORY RATE
Increased (tachypnae)

Pneumonia Acidosis (DKA, renal failure) Pulmonary embolism Respiratory failure Decreased

Intoxication/poisoning

The neurological examination focuses on the following components.

Glasgow

coma scale Breathing patterns. Pupillary responses. Eye movements. Motor responses.

GCS SCORE:
3 severe injury <8 moderate injury 9 to 12 minor injury

An abbreviated coma scale is used in the assessment of critically ill patient (primary servey) AVPU A alert V respond to voice stimulus P respond to pain U - unresponsive

Normal pupillary size, shape, and light reflexes indicate integrity of midbrain structures and a cause of coma other than a mass lesion

Medium to dilated symmetrical pupils fixed to light Structural disease of the brain stem.
Small symmetrical pupils reactive to light Metabolic diseases and drug overdose. Unequal pupil fixed to light Unilaterally enlarged pupil (>5.5 mm diameter) happens in ipsilateral 3rd nerve compression Intracranial mass lesion producing 3rd nerve palsy e.g in unilateral uncal herniation.

Morphine

extremely pin point pin point

Barbiturate Organophosphate Atropine Tricyclics

Dilated nonreacting even to physostigmine

1.VESTIBULO-OCULAR REFLEX (Caloric response)

With 10 mL of cold water douching one ear produces ipsi-lateral deviation of both eyes with a contralateral quick phase nystagmus lasting for 1 2 minutes. Use of hot water produces the opposite effect i.e. contralateral deviation with ipsilateral quick phase nystagmus. In comatose patients, the fast corrective phase of nystagmus is lost and the eyes are tonically deflected to the side irrigated with cold water or away from the side irrigated with warm water; this position may be held for 2 to 3 min.

With brainstem lesions, these vestibulo-ocular reflexes are lost or disrupted.

Elicitation of these reflexes in a comatose patient provides two pieces of information: Evidence of unimpeded function of the oculomotor nerves and of the midbrain and pontine tegmental structures that integrate ocular movements Loss of the cortical inhibition that normally holds these movements in check

Sedative or anticonvulsant intoxication serious enough to cause coma may obliterate the brainstem mechanisms for oculocephalic reactions Asymmetry in elicited eye movements remains a dependable sign of focal brainstem disease

Progressive deterioration in response to corneal touch are among the most dependable signs of deepening coma. A marked asymmetry in corneal responses indicates either an acute lesion of the opposite hemisphere or, less often, an ipsilateral lesion in the brainstem.

Restless movements of both arms and both legs and grasping and picking movements -- intact corticospinal tracts The occurrence of focal motor epilepsy usually indicates that the corresponding corticospinal pathway is intact Massive destruction of a cerebral hemisphere -focal seizures are seldom seen on the paralyzed side Definite choreic, athetotic, or hemiballistic movements indicate a disorder of the basal ganglionic and subthalamic structures, just as they do in the alert patient

Non-rhythmic jerking in single or multiple muscle groups suggests metabolic encephalopathies (hepatic chiefly).

(A ) HYPERVENTILATION

- midbrain and upper pons lesion -metabolic diseases e.g. hepatic coma, diabetes and generalised raised intracranial pressure in its early stages.
- medullary, upper cervical spinal lesion -Drug overdose and later stages of cerebral herniation.

( B ) HYPOVENTILATION

(C) CHEYNE-STOKES
-Massive supratentorial lesion -Bilateral deep-seated cerebral lesions -Metabolic disturbances Presence of CSR signifies bilateral dysfunction of cerebral structures, usually those deep in the hemispheres or diencephalon, and is seen with states of drowsiness or stupor.

( D ) ATAXIC RESPIRATION (completely irregular breathing) -Brain-stem dysfunction of a diffuse nature

Headache before the onset of coma Recurrent vomiting Severe hypertension beyond the patient's static level Subhyaloid retinal hemorrhages Papilledema develops within 12 to 24 h in cases of brain trauma and hemorrhage, but if it is pronounced, it usually signifies brain tumor or abscessi.e., a lesion of longer duration

Indicate the presence of;

Meningitis Subarachnoid hemorrhage (after 12-24 hrs in some)

Raised intracranial pressure Hypertensive changes

Subarachnoid haemorrhage
Diabetic retinopathy

Full blood counts: Infections. Biochemistry: Electrolytes, sugar, LFTs, KFTs. Arterial blood gases: Oxygen, CO2, pH, HCO3. Blood cultures. Alcohol levels. Drug screen (urine and blood)

Lumbar puncture: Infections. CT Scans in case of trauma, bleeds, hemorrhage. MRIs where possible. Thyroid function tests (rarely) Electroencephalogram (EEG) & ECG. CXR. Blood films for Malaria.

Further management depends on the cause always.

Diabetes, hepatic coma, electrolyte imbalances, endocrine causes etc: Correction of metabolic derangements. Trauma: Neurosurgery. Strokes, heart attacks, respiratory failure, hypoxia, hypothermia: Correct underlying causes. Medication/drug overdose: Specific antidotes. Meningitis and infections: Antibiotics. Raised ICP: Mannitol and Dexamethasone.

Pressure area care Care of the mouth, eyes and skin Physiotherapy to protect muscles and joints DVT prophylaxis Risks of stress ulceration of the stomach Nutrition and fluid balance Urinary catheterization Monitoring of the CVS Infection control Maintenance of adequate oxygenation

SUMMARY
ABC of life support

Oxygen and I.V access

Stabilize cervical spine

Blood glucose

Control seizures

Consider I.V glucose, thiamine, naloxone, flumazenil

Brief examination and obtain history

Investigate

Reassess the situation and plan further

THANK YOU